By using the intra-I-region recombinant mouse strain, B10.BASR1 (H-2(as4)), the immune response (Ir) genes for LDH-B and MOPC-173 were genetically and serologically separated, as assayed by T cell proliferation. Previous work demonstrated that the H-2(s) and H-2(b) strains respond to LDH-B and MOPC-173, whereas the H-2(a) and H-2(k) strains failed to respond due to haplotype-specific suppression of I-A(k)-activated T helper cells by I-E(k)-activated T suppressor cells. In the experiments reported here, B10.BASR1 mice, which lack I-E(k) expression, mounted a significant T cell proliferative response to MOPC-173 but not to LDH-B. Separation of the Ia determinants used in restricting these two antigen responses was further confirmed when pretreatment of B10.S(9R) (A(α)(s)A(β)(s)E(β)(s)J(k)) macrophages with A.TL anti-B10.HTT (anti-A(β)(s)E(β)(s)J(s)) serum absorbed with B10.BASR1 spleen cells blocked the LDH-B response but not the MOPC-173 response. Unabsorbed serum blocked both antigen responses. The primary immunogenic determinant recognized by LDH-B or MOPC-173 immune T cells was not present on both antigens, as MOPC-173-primed T cells and LDH-B-primed T cells responded only to the priming antigen. Lastly, by using the A(β) mutant strain, B6CH-2(bm12), it was shown that the Ir gene and Ia determinants affected by this mutation had no effect on the LDH-B and MOPC-173 proliferative responses. These results suggest the possibility of an intragenic recombinatorial event in either the A(α) or A(β) chain resulting in the separation of these two immune response gene functions.
|Number of pages||5|
|Journal||Journal of Immunology|
|State||Published - Dec 1 1983|